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Pathogens
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Host Phagocyte Interactions with Bacteria
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Host Phagocyte Interactions with Bacteria

A special issue of Pathogens (ISSN 2076-0817). This special issue belongs to the section "Immunological Responses and Immune Defense Mechanisms".

Deadline for manuscript submissions: closed (28 February 2022) | Viewed by 11300

Special Issue Editor

Dr. Cory Robinson

E-Mail Website
Guest Editor
Microbiology, Immunology & Cell Biology Department, School of Medicine, West Virginia University, Morgantown, WV 26506-9177, USA
Interests: host-pathogen interactions; innate immunity; early life immunity; IL-27 biology; tuberculosis; neonatal sepsis

Special Issue Information

Dear Colleagues,

As the Guest Editor of a Special Issue of Pathogens focused on host phagocyte interactions with bacteria, I invite you, as an expert in this field, to submit a manuscript for publication. This Special Issue will focus on interactions of bacterial pathogens with host phagocytes that have significant implications in bacterial persistence or clearance during human infections. This could include a wide range of activities and responses that promote antimicrobial defenses or conversely that allow bacteria to circumvent host protection. Our knowledge of host–pathogen interactions are constantly evolving. Novel mechanisms employed by host cells to eliminate bacterial pathogens and mechanisms to circumvent or exploit the host response by bacterial pathogens are continuously identified. We want to highlight new interactions that occur during infection and enrich our understanding of the interplay between host cells and pathogens.

We would like to invite the submission of original research, review articles, or short communications that report on recent progress to further expand our knowledge of these host–pathogen interactions.

Dr. Cory Robinson
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Pathogens is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • Bacterial pathogens
  • Phagocytes
  • Monocytes
  • Macrophages
  • Dendritic cells
  • Neutrophils
  • Granulocytes

Published Papers (4 papers)

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Research

Jump to: Review

11 pages, 2625 KiB  
Article
Synthetic Hexanucleotides as a Tool to Overcome Excessive Neutrophil Activation Caused by CpG-Containing Oligonucleotides
by Ekaterina A. Golenkina, Svetlana I. Galkina, Nina G. Dolinnaya, Evgenii A. Arifulin, Yulia M. Romanova and Galina F. Sud’ina
Pathogens 2021, 10(5), 530; https://0-doi-org.brum.beds.ac.uk/10.3390/pathogens10050530 - 28 Apr 2021
Viewed by 1750
Abstract
Mimicking bacterial DNA, synthetic CpG-containing oligodeoxyribonucleotides (CpG-ODNs) have a powerful immunomodulatory potential. Their practical application is mainly associated with the production of vaccines, where they are used as adjuvants, as well as in local antimicrobial therapy. CpG-ODNs act on a wide variety of [...] Read more.
Mimicking bacterial DNA, synthetic CpG-containing oligodeoxyribonucleotides (CpG-ODNs) have a powerful immunomodulatory potential. Their practical application is mainly associated with the production of vaccines, where they are used as adjuvants, as well as in local antimicrobial therapy. CpG-ODNs act on a wide variety of immune cells, including neutrophilic granulocytes. On the one hand, the stimulatory effect provides both the direct implementation of their antimicrobial and fungicidal mechanisms, and an avalanche-like strengthening of the immune signal due to interaction with other participants in the immune process. On the other hand, hyperactivation of neutrophilic granulocytes can have negative consequences. In particular, the formation of unreasonably high amounts of reactive oxygen species leads to tissue damages and, as a consequence, a spontaneous aggravation and prolongation of the inflammatory process. Under physiological conditions, a large number of DNA fragments are present in inflammation foci: both of microbial and self-tissue origin. We investigated effects of several short modified hexanucleotides on the main indicators of neutrophil activation, as well as their influence on the immunomodulatory activity of known synthetic CpG-ODNs. The results obtained show that short oligonucleotides partially inhibit the prooxidant effect of synthetic CpG-ODNs without significantly affecting the ability of the latter to overcome bacteria-induced pro-survival effects on neutrophilic granulocytes. Full article
(This article belongs to the Special Issue Host Phagocyte Interactions with Bacteria)
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14 pages, 2327 KiB  
Article
Staphylococcus aureus Induces IFN-β Production via a CARMA3-Independent Mechanism
by Yang Zhou, Shasha Zhao, Xiao Gao, Songhong Jiang, Jialu Ma, Rui Wang, Qing Li, Leiying Qin, Zhizi Tong, Junwei Wu and Jianjun Zhao
Pathogens 2021, 10(3), 300; https://0-doi-org.brum.beds.ac.uk/10.3390/pathogens10030300 - 04 Mar 2021
Cited by 6 | Viewed by 1994
Abstract
Type I interferon (IFN) induction is a critical component of innate immune response to viral and bacterial infection, including S. aureus, but whether it activates the signaling in macrophages and the regulation mechanisms is less well understood. Here we show that S. [...] Read more.
Type I interferon (IFN) induction is a critical component of innate immune response to viral and bacterial infection, including S. aureus, but whether it activates the signaling in macrophages and the regulation mechanisms is less well understood. Here we show that S. aureus infection promoted the IFN-β mRNA expression and stimulator of IFN genes (STING)/TANK-binding kinase 1 (TBK1)/interferon regulatory factor 3 (IRF3)-dependent production of IFN-β. Infection with S. aureus induced caspase recruitment domain and membrane-associated guanylate kinase-like domain protein 3 (CARMA3) expression at both the mRNA and protein levels. The heat-killed bacteria failed to trigger IRF3 phosphorylation and upregulation of CARMA3 expression. However, overexpression of CARMA3 did not affect phosphorylation of TBK1 or IRF3 in RAW264.7 cells, J774A.1 macrophages, and mouse embryonic fibroblast (MEF) cells. In conclusion, S. aureus infection induces STING/TBK1/IRF3-mediated IFN-β production in a CARMA3-independent manner. Full article
(This article belongs to the Special Issue Host Phagocyte Interactions with Bacteria)
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Review

Jump to: Research

20 pages, 3189 KiB  
Review
Mycobacterium avium Subsp. hominissuis Interactions with Macrophage Killing Mechanisms
by Norah Abukhalid, Sabrina Islam, Robert Ndzeidze and Luiz E. Bermudez
Pathogens 2021, 10(11), 1365; https://0-doi-org.brum.beds.ac.uk/10.3390/pathogens10111365 - 22 Oct 2021
Cited by 4 | Viewed by 3357
Abstract
Non-tuberculosis mycobacteria (NTM) are ubiquitously found throughout the environment. NTM can cause respiratory infections in individuals with underlying lung conditions when inhaled, or systemic infections when ingested by patients with impaired immune systems. Current therapies can be ineffective at treating NTM respiratory infections, [...] Read more.
Non-tuberculosis mycobacteria (NTM) are ubiquitously found throughout the environment. NTM can cause respiratory infections in individuals with underlying lung conditions when inhaled, or systemic infections when ingested by patients with impaired immune systems. Current therapies can be ineffective at treating NTM respiratory infections, even after a long course or with multidrug treatment regimens. NTM, such as Mycobacterium avium subspecies hominissuis (M. avium), is an opportunistic pathogen that shares environments with ubiquitous free-living amoeba and other environmental hosts, possibly their evolutionary hosts. It is highly likely that interactions between M. avium and free-living amoeba have provided selective pressure on the bacteria to acquire survival mechanisms, which are also used against predation by macrophages. In macrophages, M. avium resides inside phagosomes and has been shown to exit it to infect other cells. M. avium’s adaptation to the hostile intra-phagosomal environment is due to many virulence mechanisms. M. avium is able to switch the phenotype of the macrophage to be anti-inflammatory (M2). Here, we have focused on and discussed the bacterial defense mechanisms associated with the intra-phagosome phase of infection. M. avium possesses a plethora of antioxidant enzymes, including the superoxide dismutases, catalase and alkyl hydroperoxide reductase. When these defenses fail or are overtaken by robust oxidative burst, many other enzymes exist to repair damage incurred on M. avium proteins, including thioredoxin/thioredoxin reductase. Finally, M. avium has several oxidant sensors that induce transcription of antioxidant enzymes, oxidation repair enzymes and biofilm- promoting genes. These expressions induce physiological changes that allow M. avium to survive in the face of leukocyte-generated oxidative stress. We will discuss the strategies used by M. avium to infect human macrophages that evolved during its evolution from free-living amoeba. The more insight we gain about M. avium’s mode of pathogenicity, the more targets we can have to direct new anti-virulence therapies toward. Full article
(This article belongs to the Special Issue Host Phagocyte Interactions with Bacteria)
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15 pages, 1226 KiB  
Review
The Enigma of Low-Density Granulocytes in Humans: Complexities in the Characterization and Function of LDGs during Disease
by Brittany G. Seman and Cory M. Robinson
Pathogens 2021, 10(9), 1091; https://0-doi-org.brum.beds.ac.uk/10.3390/pathogens10091091 - 27 Aug 2021
Cited by 14 | Viewed by 3444
Abstract
Low-density granulocytes (LDGs) have been characterized as important immune cells during healthy and disease states in humans, including microbial infections, cancer, and autoimmune dysfunction. However, the classification of this cell type is similar to other immune cells (e.g., neutrophils, myeloid-derived suppressor cells) and [...] Read more.
Low-density granulocytes (LDGs) have been characterized as important immune cells during healthy and disease states in humans, including microbial infections, cancer, and autoimmune dysfunction. However, the classification of this cell type is similar to other immune cells (e.g., neutrophils, myeloid-derived suppressor cells) and ambiguous functional standards have rendered LDG identification and isolation daunting. Furthermore, most research involving LDGs has mainly focused on adult cells and subjects, leaving increased uncertainty surrounding younger populations, especially in vulnerable neonatal groups where LDG numbers are elevated. This review aims to bring together the current research in the field of LDG biology in the context of immunity to disease, with a focus on infection. In addition, we propose to highlight the gaps in the field that, if filled, could improve upon isolation techniques and functional characterizations for LDGs separate from neutrophils and myeloid-derived suppressor cells (MDSCs). This will not only enhance understanding of LDGs during disease processes and how they differ from other cell types but will also aid in the interpretation of comparative studies and results with the potential to inform development of novel therapeutics to improve disease states in patients. Full article
(This article belongs to the Special Issue Host Phagocyte Interactions with Bacteria)
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